PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “CORTICOSTERONE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Corticosterone in drinking water: altered kinetics of a single oral dose of corticosterone and concentrations of plasma sodium, albumin, globulin, and total protein.

Effects of chronic exposure to corticosterone in drinking water on corticosterone kinetics, blood chemistry, and concentrations of catecholamines in parts of brain were studied in Long-Evans rats. Rats were randomly grouped into 3 x 2 treatments (n=4), with three treatments of drinking water (tap water, or 2.5% ethanol, or 400 microg/mL of corticosterone in 2.5% ethanol) for 28 days and two treatments of gavage with a single dose of either corn oil or corticosterone 20 mg/kg on day 28. Blood samples were collected at 0, 15, 30, 60, 120, 240, 480, and 720 min after dosing to determine plasma corticosterone concentrations. Blood samples were collected for clinical pathology on day 42. Hippocampus, cerebral cortex, caudate-putamen, and pons were examined to determine concentrations of catecholamines and activities of esterases. Concentrations of plasma corticosterone before gavage of the corticosterone-drinking rats (47.61 +/- 1.13 ng/mL) were lower than the water (418.47 +/- 1.13 ng/mL) or the ethanol rats (383.71 +/- 1.13 ng/mL, P < 0.0001). Plasma corticosterone rose to peak concentrations by 15 min after gavage in all three groups of drinking rats. Corticosterone-drinking rats had concentrations of plasma corticosterone that returned to basal levels slower than water- and ethanol-drinking rats. Plasma sodium and chloride concentrations were lower in the corticosterone-drinking rats than the water-drinking rats (P < 0.01). Plasma albumin, globulin, and total protein were highest in the corticosterone-drinking rats when compared to the other groups of drinking rats (P < 0.001, P < 0.05, and P < 0.001, respectively). Corticosterone in drinking water did not affect activities of brain neurotoxic esterase, carboxylesterase, acetylcholinesterase, or concentrations of monoamines and their metabolites. A single oral dose of corticosterone reduced neurotoxic esterase activity in the cerebral cortex (P < 0.05) and increased norepinephrine concentrations in the hippocampus (P < 0.05).

Acetylcholinesterase↗

In vitro metabolism of [3H] corticosterone by mammary glands from lactating rats. Isolation and identification of 21-acyl[3H]corticosterone.

[3H] Corticosterone undergoes extensive 21-acylation on incubation with minced mammary glands from lactating rats. A purified 21-acyl [3H] corticosterone fraction was obtained by subjecting extracts of the incubated tissues to Sephadex LH-20 column chromatography followed by partitioning between n-heptane/methanol. The methanol extracts were chromatographed consecutively on columns of silica gel and C18-silanized (reverse-phase) silica gel. The radioactive product was methoximated and re-chromatographed on the reverse-phase column. Mass spectral analysis of the 21-acyl [3H] corticosterone 3,20-dimethoxime and synthetic corticosterone 21-oleate 3,20-dimethoxime suggested identity. Confirmation of the precise nature of the 21-acyl moiety was obtained by isotope dilution analysis of the underivatized radiometabolite with corticosterone 21-oleate. The composition of the 21-acyl [3H] corticosterone fraction (i.e. before extensive purification) was ascertained by isotope dilution analysis with various corticosterone esters. It appears that [3H] corticosterone 21-oleate is a major component of this fraction, representing 80% of the radioactivity; [3H] corticosterone 21-linoleate is a minor component, i.e. 8.6%. [3H] Corticosterone 21-palmitate, [3H] corticosterone 21-arachidonate, and [3H] corticosterone 21-stearate, if indeed present, constitute considerably less than 14, 6, and 2%, respectively, of the radiometabolite fraction. It is suggested that bioacylation of corticosterone serves to modulate the biological action of the glucocorticoid hormone on the mammary glands during lactation.

Animals↗

Antidepressants reverse corticosterone-mediated decrease in brain-derived neurotrophic factor expression: differential regulation of specific exons by antidepressants and corticosterone.

Earlier studies have implicated brain-derived neurotrophic factor in stress and in the mechanism of action of antidepressants. It has been shown that antidepressants upregulate, whereas corticosterone downregulates, brain-derived neurotrophic factor expression in rat brain. Whether various classes of antidepressants reverse corticosterone-mediated downregulation of brain-derived neurotrophic factor is unclear. Also not known is how antidepressants or corticosterone regulates brain-derived neurotrophic factor expression. To clarify this, we examined the effects of various classes of antidepressants and corticosterone, alone and in combination, on the mRNA expression of total brain-derived neurotrophic factor and of individual brain-derived neurotrophic factor exons, in rat brain. Normal or corticosterone pellet-implanted (100 mg, 21 days) rats were injected with different classes of antidepressants, fluoxetine, desipramine, or phenelzine, intraperitoneally for 21 days and killed 2 h after the last injection. mRNA expression of total brain-derived neurotrophic factor and of exons I-IV was measured in frontal cortex and hippocampus. Given to normal rats, fluoxetine increased total brain-derived neurotrophic factor mRNA only in hippocampus, whereas desipramine or phenelzine increased brain-derived neurotrophic factor mRNA in both frontal cortex and hippocampus. When specific exons were examined, desipramine increased expression of exons I and III in both brain areas, whereas phenelzine increased exon I in both frontal cortex and hippocampus but exon IV only in hippocampus. On the other hand, fluoxetine increased only exon II in hippocampus. Corticosterone treatment of normal rats decreased expression of total brain-derived neurotrophic factor mRNA in both brain areas, specifically decreasing exons II and IV. Treatment with desipramine or phenelzine of corticosterone pellet-implanted rats reversed the corticosterone-induced decrease in total brain-derived neurotrophic factor expression in both brain areas; however, fluoxetine reversed the decrease only partially in hippocampus. Interestingly, antidepressant treatment of corticosterone pellet-implanted rats increased only those specific exons that are increased during treatment of normal rats with each particular antidepressant. We found that although corticosterone and antidepressants both modulate brain-derived neurotrophic factor expression, and antidepressants reverse the corticosterone-induced brain-derived neurotrophic factor decrease, antidepressants and corticosterone differ in how they regulate the expression of brain-derived neurotrophic factor exon(s).

Animals↗

Developmental patterns of levels of corticosterone and of corticosterone binding in the serum of female rats: effects of ovariectomy and adrenalectomy.

Corticosterone concentrations and corticosterone binding in the serum were studied in immature female rats, using radioimmunoassay and batchwise gel equilibrium techniques. A parallel developmental pattern was found for corticosterone levels and its serum binding with a neonatal drop, followed by low levels until 12 days of age and a rise between 12 and 28 days of age. Effects of adrenalectomy, of ovariectomy, of the combined operation and of sham-operations, performed at various ages, were also studied. Adrenalectomy performed at 5 days of age did not decrease serum corticosterone concentrations within a 6-day period whereas it did in older rats. Complete disappearance of corticosterone from the blood occurred only in adult rats after combined adrenalectomy/ovariectomy. Ovariectomy and sham-operations in the younger age groups (5-15 days) caused a gradual increase in corticosterone concentration with maximal values 6 days after operation or later. The response of corticosterone secretion to these operations became more moderate and quicker, i.e. more adult-like, at 28 days of age, the age where corticosterone concentrations in intact rats also seemed to reach a plateau at an adult-like level. Corticosterone binding changed only marginally after ovariectomy or sham-operations until 28 days of age, when an increase was induced by these operations. After adrenalectomy or combined adrenalectomy/ovariectomy, however, marked increases in serum binding of corticosterone were always seen. In summary: though a parallel developmental pattern of serum corticosterone levels and corticosterone binding was seen in the maturing rat, interference with the normal condition causes divergent responses in these two parameters. Moreover, the responses vary with maturational age.

Adrenalectomy↗

Protecting embryos from stress: corticosterone effects and the corticosterone response to capture and confinement during pregnancy in a live-bearing lizard (Hoplodactylus maculatus).

Hormones in the embryonic environment, including those of the hypothalamo-pituitary-adrenal (HPA) axis, have profound effects on development in eutherian mammals. However, little is known about their effects in reptiles that have independently evolved viviparity. We investigated whether exogenous corticosterone affected embryonic development in the viviparous gecko Hoplodactylus maculatus, and whether pregnant geckos have a corticosterone response to capture and confinement that is suppressed relative to that in non-pregnant (vitellogenic) females and males. Corticosterone implants (5 mg, slow-release) administered to females in mid-pregnancy caused a large elevation of corticosterone in maternal plasma (P<0.001), probable reductions in embryonic growth and development (P=0.069-0.073), developmental abnormalities and eventual abortions. Cool temperature produced similar reductions in embryonic growth and development (P< or =0.036 cf. warm controls), but pregnancies were eventually successful. Despite the potentially harmful effects of elevated plasma corticosterone, pregnant females did not suppress their corticosterone response to capture and confinement relative to vitellogenic females, and both groups of females had higher responses than males. Future research should address whether lower maternal doses of corticosterone produce non-lethal effects on development that could contribute to phenotypic plasticity. Corticosterone implants also led to increased basking in pregnant females (P<0.001), and basal corticosterone in wild geckos (independent of reproductive condition) was positively correlated with body temperature (P<0.001). Interactions between temperature and corticosterone may have broad significance to other terrestrial ectotherms, and body temperature should be considered as a variable influencing plasma corticosterone concentrations in all future studies on reptiles.

Animals↗

Increased plasma corticosterone levels in bovine growth hormone (bGH) transgenic mice: effects of ACTH, GH and IGF-I on in vitro adrenal corticosterone production.

Previous work from our laboratory provided evidence for increased plasma corticosterone levels in mice transgenic for human and bovine growth hormone (GH). Corticosterone was elevated in both sexes, under both basal and ether-induced stress conditions. The objectives of the present study were to investigate the in vitro adrenal sensitivity to ACTH, GH and/or IGF-I in normal and bGH transgenic mice, to examine plasma corticosterone levels at different times of the day, and to determine plasma levels of ACTH in these animals. For the measurement of plasma corticosterone and ACTH levels, transgenic and normal siblings were housed 2 per cage and decapitated simultaneously within 20 seconds of the first disturbance of the cage. The corticosterone production by in vitro adrenal incubations did not differ between adrenals from normal and transgenic mice at the basal level or in the presence of different doses of ACTH. Growth hormone or IGF-I did not have any effect on corticosterone production in vitro when given alone, and did not modify the effects of ACTH on the accumulation of corticosterone production in vitro when alone, and did not modify the effects of ACTH on the accumulation of corticosterone in the media. Plasma corticosterone concentrations were higher in transgenic than in normal animals in both morning and evening. Plasma concentrations of ACTH in animals killed in the morning were sharply increased in transgenic males as compared with their normal siblings. The results indicate that increased circulating levels of corticosterone in transgenic mice are not due to a potentiation of ACTH actions by GH or IGF-I, but rather to a chronic increase in plasma ACTH levels. The increase in ACTH is presumably a reflection of GH actions in the hypothalamic-pituitary system.

Adrenal Cortex↗

[Relationship between the quality of dietary proteins and the functional status of the adrenal cortex. Variations in the content of transcortion, free corticosterone and total corticosterone in the blood plasma of rats fed with proteins of various quality].

Growing male Wistar rats were used to test in which way variations in the quality of dietary proteins (10% absorbable crude protein; casein supplemented with 4% methionine (K); casein/gelatine (1 : 3); maize gluten supplemented with 4 amino acids; and maize gluten) influenced the binding capacity of blood plasma for corticosterone, and the concentration of corticosteroid-binding globulin ("CBG"), total corticosterone, free corticosterone and albumin-bound corticosterone in blood plasma. The binding capacity of the blood plasma for corticosterone and the total concentration of corticosterone, CBG, free corticosterone and albumin-bound corticosterone were found to rise with the improving quality of the dietary proteins (r = 0.830). A close correlation was found to exist between the concentration of total corticosterone in the blood plasma and CBG. Increases in the total concentration of corticosterone in blood plasma are, in 84% of all cases, brought about by increases in CBG concentrations. In conclusion, reference is made to the significance which such results may have for the control of regulatory processes.

Adrenal Cortex↗

Impact of chronic catheterization and automated blood sampling (Accusampler) on serum corticosterone and fecal immunoreactive corticosterone metabolites and immunoglobulin A in male rats.

Jugular catheters were inserted in nine male rats under general isofluorane anesthesia and the catheters were connected to a commercially available computerized blood sampling device (Accusampler). Blood samples (150 microl) were collected every 4 h during the first 24 h after surgery and every 12 h during the following 72 h until 94 h after surgery, when the animals were killed. All fecal pellets were collected at blood sampling. Serum corticosterone and fecal concentrations of immunoreactive corticosterone metabolites and immunoglobulin A (IgA) were quantified by ELISAs. In blood, high corticosterone concentrations (>200 ng/ml) were recorded in the first samples obtained after surgery, but the concentrations decreased steadily during the day and became cyclical, showing a diurnal variation with high levels during evenings and low levels in the mornings. The automatic blood sampling itself did not result in recordable increases in serum corticosterone concentrations. The time delay between the presence of elevated corticosterone levels in blood and in feces was approximately 12 h. Fecal immunoreactive corticosterone metabolite levels remained elevated during the 94 h study period after surgery. The fecal concentrations of IgA showed substantial between-animal variation and decreased non-significantly after the surgery. Like serum corticosterone, fecal IgA showed a diurnal variation in amounts excreted, in this case with high values in the morning and low values in the evening. The concentrations of fecal corticosterone and IgA were negatively correlated in samples obtained before surgery but no correlation existed after surgery. This indicates that fecal immunoreactive corticosterone metabolites, but not IgA, constitute a good marker of acute stress. For immunoreactive corticosterone metabolites as well as for IgA, the concentration in feces correlated well with total excretion, making single fecal samplings usable as a measure of total secretion.

Acute Disease↗

Corticosterone-binding proteins and behavioral effects of high plasma levels of corticosterone during the breeding period in the pied flycatcher.

In the pied flycatcher there exists an anomaly in the relationship between cortical histology and plasma levels of corticosterone during the breeding period. In an attempt to study this anomaly, binding capacity and binding affinity of plasma corticosterone-binding proteins (CBP) were studied in free-living pied flycatchers during the early and late parts of the breeding period. Binding capacity of CBP showed a significant decrease with the progress of the breeding season in both males and females. During the early parts of the breeding season binding capacity was significantly higher in males than in females. No difference between sexes was observed during the nestling period. In males there also was a seasonal decrease in the binding affinity of CBP. The results show that there is a good relationship between periods with high plasma levels of corticosterone and its binding capacity in the blood. A second study showed that an experimentally increased plasma level of corticosterone during the nestling period drastically reduced reproductive success. Parents given silastic implants containing corticosterone fed their nestlings less frequently and produced significantly fewer fledglings than did controls. Unlike the control birds, the body weight of the corticosterone-implanted birds did not decrease during the nestling period. Birds given corticosterone implants in which one small hole had been punched, in order to facilitate diffusion of corticosterone, all abandoned their territories and, consequently, these parents produced no fledglings. Thus, the results show that an elevation of plasma levels of corticosterone in adult pied flycatchers during the nestling period affects parental as well as territorial behavior.

Animals↗

The release of corticosterone and a corticosterone-binding protein by incubated rat adrenal slices.

Stimulation of incubated rat adrenal slices with ACTH(1-24) resulted in an increase in the release of both corticosterone and specific corticosterone-binding protein into the incubation medium. The release of corticosterone and binding protein was dose and calcium dependent with adrenals from animals pretreated with betamethasone. While the secretion of corticosterone was continuous throughout the incubation period, there appeared to be a limit to the increase in binding capacity. The specificity of steroid binding to the adrenal protein showed a similar profile to that of corticosteroid-binding globulin (CBG) in rat serum. A Western blot analysis using anti-rat CBG as the primary antiserum, showed that the adrenal protein was not CBG. [3H]corticosterone binding with disc electrophoresis, run at 2 degrees C, gave a single peak with approximately the same Rf value for rat serum, purified CBG, and adrenal incubate; at 22 degrees C peaks were only seen for rat serum or purified CBG. The data presented provides further evidence for the existence of a specific corticosterone-binding protein of adrenal origin released in conjunction with corticosterone. The adrenal protein would appear to have a lower affinity for corticosterone than does CBG, and to be functionally more labile. It is possible that the adrenal protein may be CBG that has been internalized, modified and released with corticosterone.

Adrenal Glands↗

Quantitative relationships between the suppression of selected immunological parameters and the area under the corticosterone concentration vs. time curve in B6C3F1 mice subjected to exogenous corticosterone or to restraint stress.

The neuroendocrine response to stressors increases the concentration of several endogenous mediators, some of which are immunosuppressive. However, quantitative aspects of these effects have been overlooked. Although it should be possible to predict the degree of suppression of particular immunological functions by measuring the concentrations of stress-related mediators such as corticosterone, this cannot be done with data presently available. This study was designed to develop regression models to predict the relationship between the area under the corticosterone concentration vs. time curve (AUC) and two immunological parameters. Models were developed using mice treated with exogenous corticosterone and mice subjected to various periods of restraint stress. The latter treatment was included to determine if the effects of corticosterone were different from those of corticosterone in association with the other mediators induced in a restraint-stress response. Models relating corticosterone AUC to expression of MHC class II proteins on splenocytes were very similar, whether the corticosterone was exogenous or produced as part of a restraint-stress response. This was also true for splenic natural killer (NK) cell activity. However, MHC class II expression was more sensitive to the effects of corticosterone or restraint than was NK cell activity. The corticosterone and restraint models predicted the previously published effect of a chemical stressor (ethanol) on MHC class II expression, but neither model predicted the suppression of NK cell activity by ethanol. These results have mechanistic implications, which are discussed in the context of previous studies. The quantitative models described here should be useful in determining and predicting the stress-related portion of chemical-induced immunosuppression. In addition, these models provide quantitative data essential for a complete understanding of stress-induced immunosuppression.

Animals↗

Augmented ACTH responses to stress in adrenalectomized rats replaced with constant, physiological levels of corticosterone are partially normalized by acute increases in corticosterone.

Adrenalectomized rats replaced with constant, physiological levels of corticosterone via a subcutaneous pellet (Pellet) have normal basal morning ACTH but exhibit enhanced and prolonged ACTH responses to stress vs. sham-operated (Sham) rats. It has not been determined if the lack of either stress-induced or circadian increases in corticosterone, both of which are missing in Pellet rats, may account for this enhanced response. To test the extent to which stress-associated increases in corticosterone alone can normalize stress-induced hypersecretion of ACTH, we approximated endogenous secretion by injecting additional corticosterone in Pellet rats via an indwelling subcutaneous cannula, 5 min before hypoxia stress (10% O2). A corticosterone dose of 666 micrograms/kg (Pellet+B), but not 333 micrograms/kg (Pellet+Low B), produced plasma corticosterone levels comparable to those in Shams and normalized stress-induced but not post-stress plasma ACTH. Administration of the type II corticosteroid receptor antagonist RU 38486 30 min before corticosterone reversed this inhibition. We conclude that enhanced ACTH responses to stress in Pellet rats result in large part from lack of type II receptor-mediated feedback inhibition by corticosterone increases during stress, although prior circadian increases in corticosterone may also be required.

Adrenalectomy↗

Relationship of plasma corticosterone and adrenal cholesterol and corticosterone to the production of soft-shelled and shell-less eggs.

Two experiments were conducted to determine if plasma corticosterone and adrenal cholesterol and corticosterone levels differed among hens that laid soft-shelled (SS) or shell-less (SL) eggs when compared with hard-shelled (HS) egg layers. For Experiment 1, four groups of White Leghorn hens were bled at 22 to 34 weeks of age in the morning (0600 to 1200 hr) and at 66 to 74 weeks of age in the morning and evening (1500 to 1900 hr). Group 1 consisted of birds that had just laid SS or SL eggs, whereas Group 2 hens had SS or SL eggs in utero. Groups 3 and 4 represented hens with HS eggs in their uteri and hens that had just laid HS eggs, respectively. For Experiment 2, adrenal cholesterol and corticosterone levels were assayed in high (18+%) and low (0%) incidence SS plus SL egg layers at 73 and 78 weeks of age. Both younger and older hens that laid SS or SL eggs in the morning had similar plasma corticosterone concentrations when compared to HS egg layers. Morning plasma corticosterone levels were significantly higher among hens that laid an egg when compared to hens with eggs in utero, regardless of whether the egg was SS, SL, or HS. However, plasma corticosterone levels of hens producing SS or SL eggs in the evening were significantly higher than levels of hens that laid evening HS eggs. Evening HS egg layers demonstrated the oviposition related peak in plasma corticosterone, but concentrations were 1 ng/ml higher among the evening SS or SL egg layers. Adrenal cholesterol and corticosterone concentrations were similar between high and low incidence SS plus SL layers at either age. It is postulated that evening production of SS or SL eggs is a consequence of elevated plasma corticosterone.

Adrenal Glands↗

Plasma concentrations of LH, progesterone, and corticosterone during ACTH- and corticosterone-induced ovulation in the hen (Gallus domesticus).

Corticosterone and ACTH were injected either 6 hr after ovulation of a mid-sequence follicle or 14 hr before the first ovulation of a sequence. Ovulation was not induced by injection of either hormone given 6 hr after ovulation but 12 of 15 hens injected with 1.5 mg of corticosterone and 6 of 13 hens injected with 10 IU of ACTH given 14 hr before the first ovulation of a sequence ovulated within 8 hr. Injection of either ACTH or corticosterone 6 hr after a mid-sequence ovulation was followed by a decline in the concentration of LH, whereas the concentration of progesterone remained stable. The concentration of both LH and progesterone was increased during 1-5 hr before an ovulation induced by an injection of either ACTH or corticosterone given 14 hr before the first ovulation of a sequence. The increase in the plasma concentration of corticosterone which was required to induced ovulation with either hormone was identical and not within the normal physiological range. It was concluded that the ovulation-inducing action of ACTH was mediated by its effect on corticosterone production and/or secretion by the adrenal gland, that a mature follicle capable of progesterone secretion must exist within the ovary before an injection of either ACTH or corticosterone can induce ovulation, and that the ovary is the most probable target tissue for corticosterone in the context of its ovulation-inducing action.

Adrenocorticotropic Hormone↗

The effects of acute and chronic administration of corticosterone on rat behavior in two models of fear responses, plasma corticosterone concentration, and c-Fos expression in the brain structures.

The aim of this paper was to examine changes in rat emotional behavior, and to find the brain structures, which are involved in the mediation of behavioral effects, related to the repeated administration of glucocorticoids. The effects of acute and chronic pretreatment of rats with two doses of corticosterone (5 and 20 mg/kg) were analyzed in two models of fear responses: neophobia-like behavior in the open field test, and freezing reaction in the conditioned fear test. Behavioral effects of repeated glucocorticoid administration were compared to changes in blood total corticosterone concentration, and expression of immediate early gene (c-Fos) in brain structures. It was found that acute administration of corticosterone (90 min before tests) enhanced rat exploratory behavior, and decreased freezing reaction. On the other hand, repeated administration of corticosterone (for 25 days, the final injection 90 min before contextual fear conditioning training) decreased plasma corticosterone concentration, inhibited exploratory behavior, enhanced freezing responses on retest and produced a complex pattern of changes in c-Fos expression, stimulated by exposure of rats to the aversively conditioned context. Aversive context induced c-Fos in the magnocellular neurons of the hypothalamic paraventricular nucleus (mPVN), dentate gyrus (DG), cingulate cortex area 1 (Cg1), and primary motor cortex (M1). In rats chronically treated with corticosterone this effect was attenuated in the mPVN and DG, enhanced in the M1, and additionally observed in the CA1, CA2 layers of the hippocampus, and in the central nucleus of amygdala (CeA), in comparison to control animals not subjected to contextual fear test. In sum, the present data suggest that chronic corticosterone treatment enhances the activity of primary motor cortex and CeA with subsequent improvement of memory of aversive events, and simultaneously stimulates a negative feedback mechanism operating in PVN with ensuing decrease in blood corticosterone concentration.

Animals↗

Is corticosterone-mediated phenotype development adaptive? Maternal corticosterone treatment enhances survival in male lizards.

Hormones are an important interface between genome and environment, because of their ability to modify the phenotype. More particularly, glucocorticoids are known to affect both morphological, physiological and behavioral traits. Many studies suggest that prenatal stress (associated with an elevation of corticosterone) has deleterious effects on offspring, an altered physiology resulting in retardation of fetal growth and higher percentage of dead neonates. In this study, we investigate the consequences of an artificial increase of corticosterone in pregnant female Lacerta vivipara on two important fitness components: growth and survival. Do stressed females decrease or enhance offspring survival? In 2000 and 2001, we collected pregnant females from four populations of the Cevennes and kept them in the laboratory until parturition. We applied a corticosterone solution daily onto the backs of some females. A similar solution, but without corticosterone, was applied to the remaining females as a control. Immediately after birth, we measured juveniles' morphological characteristics and released them on the field. In September of the year of release and in May of the following year, we recaptured offspring to estimate growth and survival. The elevation of the corticosterone level in pregnant females L. vivipara had a profound impact on juvenile traits. The size, the body condition and the growth of juveniles were decreased by the corticosterone treatment. In contrast, in male juveniles, survival was higher for juveniles from corticosterone-treated females than from placebo females. Thus, corticosterone does not seem to have detrimental effects on offspring survival, suggesting that it may have an adaptive function.

Adaptation, Physiological↗

The effect of transdermal corticosterone application on plasma corticosterone levels in pregnant Lacerta vivipara.

Relationships between hormones and behaviour can be explored by altering endogenous hormone levels, often through implantation of silastic tubing or osmotic pumps filled with a hormone or its agonists or antagonists. However, organisms in sensitive life-history stages (such as pregnancy) may be adversely affected by the surgical procedures associated with these manipulations, necessitating use of non-invasive techniques. We demonstrate that the application of a sesame oil-corticosterone mixture to the skin of pregnant female common lizards (Lacerta vivipara) elevates plasma levels of the hormone. Pregnant female L. vivipara were captured and treated daily for 1-20 days with the sesame oil-corticosterone mixture (experimental group) or with vehicle only (control group). Blood samples were collected and analyzed for corticosterone by radioimmunoassay. Baseline plasma corticosterone levels were elevated within 1 h in the experimental group. Similar levels ( approximately 145 ng/ml) were found over the subsequent 2 days, and by day 5 had risen significantly higher ( approximately 281.9 ng/ml), where they remained for the duration of the experiment. These increases are comparable to those found in other species using related techniques. No significant changes in plasma corticosterone levels occurred in the control group. Finally, corticosterone levels also were determined for untreated females that were captured, held overnight, sampled, and released to access to the natural range of basal corticosterone levels. Basal plasma levels of corticosterone in pregnant females varied among individuals independently of female body size or corpulence.

Administration, Cutaneous↗